基于可视化图形特征融合的蛋白质组学质谱数据分析

近年来,对蛋白质组学质谱数据进行模式识别成为癌症诊断的一种新方法,由此发现的新生物标记物已经成功用于多种重大疾病的早期预测.这种方法的两个难点是:如何提取能够明显区分不同类别的特征,如何有效处理谱数据中大量的特征.本文提出基于多元图形特征融合的方法对蛋白质组学质谱高维数据进行可视化降维处理.在对质谱数据进行必要的预处理后,选择部分原始特征并将其映射到多元图表示域.通过多层递阶图形特征选择与提取得到最终的多元图癌症诊断模板.采用国际公开卵巢癌高通量数据集进行验证,得到了较好的分类效果.     

HPV病毒及其疫苗的研究进展

人乳头瘤病毒（HPV）是引起宫颈癌的主要病因,HPV疫苗的研制成为近年来研究热点.主要对HPV病毒的结构、HPV疫苗不同类型及其优缺点进行综述,最后针对目前HPV疫苗面临的安全、有效、成本等问题提出展望.     

癌症的基因治疗

癌症是导致人类死亡的疾病之一,癌症的治疗广泛地引起了人们的关注,癌症的基因治疗是近年来癌症治疗的新突破．本文从导入抑癌基因的基因治疗,针对癌基因的反义疗法,“自杀”基因,导入细胞因子的基因治疗,转入耐药基因的治疗几个方面介绍了癌症基因治疗的新进展．     

清热解毒活血化瘀复方对大鼠胃癌前病变的抑制及对NF-κBmRNA表达的影响

目的：观察清热解毒、活血化瘀复方对胃癌癌前病变及NF—κBmRNA表达的影响。方法：采用MNNG对Wistar雄性大鼠灌胃法建立胃癌癌前病变动物模型,随机将造模成功的50只雄性大鼠分为模型组、维酶素组、中药高、中、低剂量组,每组10只,各组给予相应的处理每天灌胃一次,每次2mL,连续12周后观察各组大鼠的一般情况、胃粘膜病变组织的病理变化以及NF—κBmRNA表达的变化。结果：清热解毒、活血化瘀复方组与模型组相比较IM与ATP的发生率明显降低（P〈0．01）,与维酶素组相比较中药中、高剂量组IM与ATP的发生率显著降低（P〈0．05）;各中药治疗组与模型组相比,NF-κBmRNA的表达明显下降（P〈0．05）,中药中、高剂量组优于维酶素组（P〈0．05）,而中药低剂量组与维酶素组差异无统计学意义（P〉0．05）。结论：清热解毒、活血化瘀复方不仅能够明显改善胃粘膜癌前病变的病理状态,而且同时能够明显降低NF—κB炎症通路的表达和激活,可能为其抗炎、抗癌前病变的重要机制之一。     

早期发现子宫颈癌9例临床分析

目的探讨子宫颈癌早期发现、早期诊断及早期治疗的影响因素和意义.方法结合9例早期子宫颈癌患者的临床资料分析和相关文献回顾.结果与结论阴道镜检查对宫颈癌早期发现意义重大,对可疑患者建议重复多次行病理组织活检;宫颈醋酸白色上皮、粗镶嵌和点状血管是原位癌三联征,对早期发现宫颈癌也具有重要意义.     

Cancer and blood coagulation

In human patients, blood coagulation disorders often associate with cancer, even in its early stages. Recently, in vitro and in vivo experimental models have shown that oncogene expression, or inactivation of tumour suppressor genes, upregulate genes that control blood coagulation. These studies suggest that activation of blood clotting, leading to peritumoral fibrin deposition, is instrumental in cancer development. Fibrin can indeed build up a provisional matrix, supporting the invasive growth of neoplastic tissues and blood vessels. Interference with blood coagulation can thus be considered as part of a multifaceted therapeutic approach to cancer. Received 30 November 2005; received after revision 7 February 2005; accepted 8 February 2006     

Peutz-Jeghers syndrome: clinicopathology and molecular alterations

Peutz-Jeghers syndrome (PJS, OMIM 175200) is an unusual inherited intestinal polyposis syndrome associated with distinct peri-oral blue/black freckling [1–9]. Variable penetrance and clinical heterogeneity make it difficult to determine the exact frequency of PJS [4]. PJS is a cancer predisposition syndrome. Affected individuals are at high risk for intestinal and extra-intestinal cancers. In 1997, linkage studies mapped PJS to chromosome 19p [10, 11], and subsequently a serine/threonine kinase gene defect (LKB1) was noted in a majority of PJS cases [12, 13]. A phenotypically similar syndrome has been produced in an LKB1 mouse knockout model [14–18]. Several PJS kindred without LKB1 mutations have been described, suggesting other PJS loci [19–22]. The management of PJS is complex and evolving. New endoscopic technologies may improve management of intestinal polyposis. Identification of specific genetic mutations and their targets will more accurately assess the clinical course, and help gage the magnitude of cancer risk for affected individuals. Received 20 February 2006; received after revision 5 May 2006; accepted 15 June 2006     

Antizyme inhibitor: mysterious modulator of cell proliferation

In contrast to the considerable interest in the oncogene ornithine decarboxylase (ODC) and in the family of antizymes with regard to cell proliferation and tumorigenesis, the endogenous antizyme inhibitor (AZI) has been less well studied. AZI is highly homologous to the enzyme ODC but does not possess any decarboxylase activity. Elevated ODC activity is associated with most forms of human malignancies. Antizymes bind ODC, inhibit ODC activity and promote the ubiquitin-independent degradation of ODC. Consequently they are proposed as tumor suppressors. In particular, the most studied member of the antizyme family, antizyme 1, has been demonstrated to play a role in tumor suppression. AZI inactivates all members of the antizyme family, reactivates ODC and prevents the proteolytic degradation of ODC, which may suggest a role for AZI in tumor progression. Received 9 December 2005; received after revision 13 April 2006; accepted 1 June 2006